Leader delegation and trust in global software teams

Virtual teams are an important work structure in global software development. The distributed team structure enables access to a diverse set of expertise which is often not available in one location, to a cheaper labor force, and to a potentially accelerated development process that uses a twenty-four hour work structure. Many software teams are partially distributed, that is, part of the team is colocated. Such partially distributed global software teams are an important work structure in software development projects. However, little is known about what affects or improves team members’ motivation and job satisfaction in the partially distributed environment. This study investigates the effects of leader delegation to sub-teams and trust between sub-teams on global software team members’ motivation and job satisfaction. It proposes a research framework based on specific hypotheses regarding these effects. A survey instrument was created and a pilot study conducted on student project teams in two U.S. universities. In addition, a study combining interviews and a survey distribution using industry software development teams was also conducted. The studies found that team competence predicts leader delegation to a sub-team in global software projects. Leader delegation related to teamwork process improves team members’ motivation and satisfaction with the leader. However, leader delegation may also generate negative consequences for the sub-teams, such as anxiety and pressure. Cultural distance and geographical distance impair trust development between members across sub-teams. Temporal distance causes conflicts related to excessive overtime and meeting scheduling. Trust in sub-teams is critical to improving motivation in a global software project. In addition, this study explores the impacts of language differences and software engineering profession culture on global software team members’ interactions. Suggestions are proposed for how to shape delegation strategies in partially distributed global software projects and how to improve team members’ trust in each other and their motivation. This work provides important findings for organizations interested in developing leadership skills for global software teams and retaining IT professionals at distributed sites

ANO1 as a marker of oral squamous cell carcinoma and silencing ANO1 suppresses migration of human SCC-25 cells

Objectives: The purpose of this study is to confirm that ANO1 correlates with occurrence and metastasis of OSCC. Study Design: Immunohistochemistry was used to detect the expression of ANO1 in 160 specimens of OSCC and normal tissues. Lentiviral silencing ANO1 was used in scc-25 cell line to study the cell migration and cell detachment. Results: Immunohistochemical staining revealed that ANO1 was expressed in a large majority (132 out of 160, 82.5%) of OSCC specimens and that the rate of ANO1 expression in OSCC was significantly higher than that of normal tissue ( P <0.05); The rate of ANO1 expression was higher in metastatic tumors than in non-metastatic tumors, and the difference was significant ( P <0.05). The results of cell migration assay showed that the percent - age of cells through the membrane was 26.61 ±0.81 in assay group, and 54.26 ±3.74 in control group, respectively (t =-16.22, P <0.0001). The results of cell detachment assay showed that the percentage of cells detachment was 37.42 ±0.90 in assay group, and 87.38 ±1.59 in control group, respectively (t=-62.34, P <0.0001). The results of wound healing assay showed the assay group had a reduced migration rate compared with the control group in 32 h (F=1038.78, P <0.0001). Wound closure was no significantly different between the assay and control cells when DIDS was used in wound healing assay (F=4.61, P >0.05). Conclusions: Our study shows that abnormal expression of ANO1 correlated with the occurrence and metastasis of OSCC in clinical specimens and that silencing ANO1 greatly reduced migration ability of scc-25 cells. Calcium activated chloride channel activity of ANO1 promoted the cell migration. Thus, ANO1 could represent a new diagnostic biomarker and a potentially important therapeutic target of OSCC

Protection and regeneration of traditional buildings based on BIM:A case study of Qing Dynasty tea house in Guifeng Village

In the context of China\u27s rapid urbanization, large quantities of traditional buildings are disappearing. How to efficiently and intuitively protect these traditional buildings is an important issue being faced. Taking a Qing Dynasty tea house in Guifeng Village as an example, this paper applies information collection, processing and saving in a Building Information Model (BIM) for traditional buildings. It focuses on the application of BIM in traditional buildings’ surveying and creating 3D virtual models of a tea house with Revit Architecture, in order to provide a new method for the protection and regeneration of traditional buildings

Targeting the BRD4/FOXO3a/CDK6 Axis Sensitizes AKT Inhibition in Luminal Breast Cancer

BRD4 assembles transcriptional machinery at gene super-enhancer regions and governs the expression of genes that are critical for cancer progression. However, it remains unclear whether BRD4-mediated gene transcription is required for tumor cells to develop drug resistance. Our data show that prolonged treatment of luminal breast cancer cells with AKT inhibitors induces FOXO3a dephosphorylation, nuclear translocation, and disrupts its association with SirT6, eventually leading to FOXO3a acetylation as well as BRD4 recognition. Acetylated FOXO3a recognizes the BD2 domain of BRD4, recruits the BRD4/RNAPII complex to the CDK6 gene promoter, and induces its transcription. Pharmacological inhibition of either BRD4/FOXO3a association or CDK6 significantly overcomes the resistance of luminal breast cancer cells to AKT inhibitors in vitro and in vivo. Our study reports the involvement of BRD4/FOXO3a/CDK6 axis in AKTi resistance and provides potential therapeutic strategies for treating resistant breast cancer

Aggravated myocardial infarction-induced cardiac remodeling and heart failure in histamine-deficient mice

Histamine has pleiotropic pathophysiological effects, but its role in myocardial infarction (MI)-induced cardiac remodeling remains unclear. Histidine decarboxylase (HDC) is the main enzyme involved in histamine production. Here, we clarified the roles of HDC-expressing cells and histamine in heart failure post-MI using HDC-EGFP transgenic mice and HDC-knockout (HDC−/−) mice. HDC+CD11b+ myeloid cell numbers markedly increased in the injured hearts, and histamine levels were up-regulated in the circulation post-MI. HDC−/− mice exhibited more adverse cardiac remodeling, poorer left ventricular function and higher mortality by increasing cardiac fibrogenesis post-MI. In vitro assays further confirmed that histamine inhibited heart fibroblast proliferation. Furthermore, histamine enhanced the signal transducer and activator of transcription (STAT)-6 phosphorylation level in murine heart fibroblasts, and the inhibitive effects of histamine on fibroblast proliferation could be blocked by JAK3/STAT6 signaling selective antagonist. STAT6-knockout (STAT6−/−) mice had a phenotype similar to that of HDC−/− mice post-MI; however, in contrast to HDC−/− mice, the beneficial effects of exogenous histamine injections were abrogated in STAT6−/− mice. These data suggest that histamine exerts protective effects by modulating cardiac fibrosis and remodeling post-MI, in part through the STAT6-dependent signaling pathway

PRL3-zumab, a first-in-class humanized antibody for cancer therapy

Novel, tumor-specific drugs are urgently needed for a breakthrough in cancer therapy. Herein, we generated a first-in-class humanized antibody (PRL3-zumab) against PRL-3, an intracellular tumor-associated phosphatase upregulated in multiple human cancers, for unconventional cancer immunotherapies. We focused on gastric cancer (GC), wherein elevated PRL-3 mRNA levels significantly correlated with shortened overall survival of GC patients. PRL-3 protein was overexpressed in 85% of fresh-frozen clinical gastric tumor samples examined but not in patient-matched normal gastric tissues. Using human GC cell lines, we demonstrated that PRL3-zumab specifically blocked PRL-3(+), but not PRL-3(–), orthotopic gastric tumors. In this setting, PRL3-zumab had better therapeutic efficacy as a monotherapy, rather than simultaneous combination with 5-fluorouracil or 5-fluorouracil alone. PRL3-zumab could also prevent PRL-3(+) tumor recurrence. Mechanistically, we found that intracellular PRL-3 antigens could be externalized to become “extracellular oncotargets” that serve as bait for PRL3-zumab binding to potentially bridge and recruit immunocytes into tumor microenvironments for killing effects on cancer cells. In summary, our results document a comprehensive cancer therapeutic approach to specific antibody-targeted therapy against the PRL-3 oncotarget as a case study for developing antibodies against other intracellular targets in drug discovery